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To compare the effects of dexmedetomidine (DEX) pretreatment, posttreatment, and whole-course pumping on myocardial protection during cardiac valve replacement.One hundred and twenty patients undergoing cardiac valve replacement were randomly divided into the follow groups: DEX pretreatment (D1 group), DEX posttreatment (D2 group), DEX whole-course pumping (D3 group), and Control (C group). The concentrations of cardiac troponin I (cTnI), malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), rate of spontaneous heart rebound after aortic opening, time to heart rebound, incidence of arrhythmia, and use of sufentanil and vasoactive drugs were recorded.Compared with group C, the concentrations of cTnI, MDA, and TNF-α in the D1, D2, and D3 groups were lower, especially in the latter. The time to heart rebound was prolonged in all three groups (P0.05). The rate of automatic rebound was increased (P0.05) while the incidence of arrhythmia was decreased (P0.05) in all groups compared with group C. Group D3 had the highest rate of automatic rebound and the lowest incidence of arrhythmia. Compared with groups C and D2, the use of sufentanil and dopamine was lower in groups D1 and D3 (P0.05), especially in the latter.During cardiac valve replacement, DEX pretreatment, posttreatment, and whole-course pumping could have myocardial protective effects. The latter showed better effects.

Background: Mechanical ventilation using lower tidal volume ventilation with associated hypercapnia is supported to avoid ventilator-induced lung injury, but the underlying mechanism is not clear. This study was intended to explore whether low tidal volume ventilation with associated hypercapnia would ameliorate pneumoperitoneum-induced lung injury and whether this protection strategy might work through mediating inflammation and oxidative stress via TLR 4 signaling pathway. Materials and methods: 50 anesthetized Wistar Rats were randomized to be mechanically ventilated for 4 h at 7 groups: Group A, ventilated with 12 ml/kg; Group B, similar to Group A but injected with LPS (Toll receptor 4 agonist); Group C, similar to Group A but injected with Pam3Cys (Toll receptor 2 agonist); Group D, ventilated with 12 ml/kg and subjected to pneumoperitoneum; Group E, ventilated with 6 ml/kg and subjected to pneumoperitoneum; Group F, similar to Group E but injected with LPS; Group G, similar to Group E but injected with Pam3Cys. After animals were killed, indices of lung Injury, inflammation markers and oxidative stress markes of the lungs tissues, bronchoalveolar lavage fluid and blood were assessed. Results: The group subjected to pneumoperitoneum (Group D) had elevated values of indices of lung Injury, inflammation oxidative stress markers compared with the controls (Group A). The low tidal volume ventilation group (Group E) had significantly decreased values of markers of lung Injury, inflammation and oxidative stress compared with the high tidal volume ventilation group (Group D). LPS treatment reversed all the results of Group E, while Pam3Cys treatment had no significant effect. Conclusions: Low tidal volume ventilation with associated hypercapnia ameliorated pneumoperitoneum-induced lung injury by reducing TLR 4-mediated inflammation and oxidative stress.